Resumen

In 1997, Welch identified in a child the hyperprostaglandin E syndrome, which is characterized by raised calcitriol, hypercalciuria and urinary hyperexcretion of PGE2. Welch hypothesized that hyperprostaglandin E increases the synthesis of calcitriol, increasing Ca absorption which causes hypercalciuria. In this work analyze the existence of the clinical syndrome reported by Welch. We review the experimental and clinical bibliography on the relationship between prostaglandins (PG) E and the calcitriol synthesis. Observations in vivo, in vitro and in many clinical studies, showed that PG E, increased the calcitriol synthesis. The review of medical literature proved that the PG E increases the synthesis of calcitriol and reproduces the hyperprostaglandin E syndrome. This has been rarely mentioned. The hyperprostaglandin E syndrome exists in children. This syndrome could be present as a unic entity or superimposed to other pathologies